Hemichorea associated with subcortical border-zone infarction and middle cerebral artery stenosis

Involuntary movement disorders sometimes occur after a stroke. One study reported that 1% of 2,500 stroke patients presented involuntary movement disorders [1]. These involuntary movement disorders include hypokinetic movement disorders and hyperkinetic movement disorders. Among these, hemichorea has been reported as the most common post-stroke hyperkinetic movement disorder [1,2]. Post-stroke hemichorea is most commonly associated with a lesion in basal ganglia and related structures. In addition, several cases caused by cortical lesions have been reported. However, acute hemichorea associated with the lesions confined to subcortical white matter were very rarely reported [2,3]. We report a patient with subcortical border-zone infarction and middle cerebral artery (MCA) stenosis presenting with contralateral hemichorea. A 79 years-old female presented with hyperkinetic movement of the left arm and leg, accompanied by dysarthria, which first occurred 10 days ago. She had no previous or family history and was not taking any medications. At presentation, she appeared alert, and cooperative. Her muscle strength and sensory functions were normal. Deep-tendon reflexes were also normal and the Babinski sign was not elicited. There were involuntary, irregular and unpredictable muscle movements in her left arm and leg, consistent with chorea, more severe in the upper extremity. This involuntary movement was exaggerated during the intentional movement of the limb, and disappeared during sleep. Laboratory tests, including blood sugar, uric acid, serum electrolytes, liver enzyme levels, and thyroid hormone levels, were all normal. She had normal cardiac rhythm on an electrocardiogram. Diffusion-weighted brain magnetic resonance imaging (MRI) showed several scattered high signal intensities in the subcortical white matter of right frontal and parietal lobes, consistent with cortical border-zone area (between right anterior cerebral artery (ACA) and MCA and between right MCA and posterior cerebral artery (PCA)) (Fig. 1). Brain magnetic resonance angiography (MRA) showed a focal severe stenosis at right proximal M1 segment and mild stenosis at left proximal M1 segment (Fig. 1). She was treated with antiplatelet agents, atorvastatin and hydration with normal saline and clonazepam for chorea. Her symptoms improved noticeably from the very next day. Hemichorea is usually caused by brain lesions involving basal ganglia structures, drugs, infection of